Biochemistry of Diabetes and Atherosclerosis by Takashi Nagasawa, Nobuaki Tabata (auth.), James S. C.

By Takashi Nagasawa, Nobuaki Tabata (auth.), James S. C. Gilchrist, Paramjit S. Tappia, Thomas Netticadan (eds.)

Diabetes is an autoimmune, inflammatory affliction affecting many various organ platforms and displaying either basic and secondary defects. simply because diabetes impacts quite a lot of mobile platforms, a multidisciplinary attempt has been fixed over the last a number of a long time utilizing quite a lot of investigative strategies and methodologies in an effort to establish molecular mechanisms liable for mobile disorder. simply because fundamental defects at quite a few degrees of sub-cellular signaling, intracellular calcium dealing with, protein expression and effort rules are usually a major end result of diabetes.

This quantity is a compilation of latest multidisciplinary study that may develop our present figuring out of diabetes and heart problems in addition to give you the foundation for the improvement of novel healing interventions.

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9. 10. II . 12. tivation of glycogen synthase kinase 3 in L6 muscle cells. Diabetes 47 : 1006-1013,1998 Han X, Bonen A: Epinephrine translocates GLUT-4 but inhibits insulin-stimulated glucose transport in rat muscle . Am J Physiol274: E700E704, 1998 Doenst T, Taegtmeyer H: Alpha-adrenergic stimulation mediates glucose uptake through phosphatidylinositol3-kinase in rat heart. Circ Res 84:467-474,1999 Shimizu Y, Kielar D, Minokoshi Y, Shimazu T: Noradrenaline increases glucose transport into brown adipocytes in culture by a mechanism different from that of insulin.

We have previously reported significantly lower glut 4 expression in Zucker obese rat hearts, combined with a lower affinity of glut 4 as measured by the cytochalasin B binding method [20]. Both these conditions may contribute to the lower basal glucose uptake in these hearts . Ol vs insulin F ig. 5. Comparative effects of insulin (I ) and vanadate (V) on 2-DG up- take and PKB phosphorylation in cardiomyocytes from control and obese Zucker rats. The cells were incubated with the addition of 100 nM insulin or 5 mM vanadate and 2-DG uptake determined as described in 'Materials and methods'.

Lack of recovery from stunning and absence of preconditioning protection in diabetes: An explanation based on KATP channel dysfunction Sarcolemmal KATP channels are important structures present in many tissues and are of particular interest in the cardiovascular system where they have been suggested to playa cardioprotective role during ischemic episodes [23], their activation increasing the outward potassium current and reducing action potential duration (APD) [36,37]. It has been speculated that their cardioprotection would be attained through this action potential shortening, decreasing the time of Ca 2+ influx through Ca 2+ voltage dependent channels and avoiding the deleterious effects of Ca2+ overload [36, 37].

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